Analysis Tools
cellular
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• primary neurons show an increase in the number of total mitochondria and damaged mitochondria
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• tamoxifen-treated murine embryonic fibroblasts (MEFs) show elevated ratio of LC3B-II to LC3B-1, indicating elevated autophagosome formation and accumulation after treatment with Earles Balanced Salt Solution (EBSS)
• tamoxifen-treated MEFs treated with EBSS and the autophagic inhibitor, bafilomycin A1, show unchanged ratio of LC3B-II/LC3B-I, suggesting no effect on induction of autophagic flux but more likely autophagosome degradation
• 13-cis retinoic acid can still rescue the autophagic defects when tamoxifen-treated primary neurons are treated with AGN 194310, a RAR pan-inhibitor
• however, docosahexaenoic acid, an agonist of RXR, does not rescue the autophagic defects in tamoxifen-treated primary neurons
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• primary neurons treated with tamoxifen show an increase in the number of mitochondria in autophagosomes indicating that damaged mitochondria accumulate rather than undergo autophagic degradation
• primary neurons treated with tamoxifen and then 13-cis retinoic acid show restoration of the impaired mitophagic activity
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• tamoxifen-treated primary neurons show an increase in mitochondrial reactive oxygen species (ROS) levels
• primary neurons treated with tamoxifen and then 13-cis retinoic acid show a decrease in mitochondrial ROS accumulation
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homeostasis/metabolism
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• tamoxifen-treated murine embryonic fibroblasts (MEFs) show elevated ratio of LC3B-II to LC3B-1, indicating elevated autophagosome formation and accumulation after treatment with Earles Balanced Salt Solution (EBSS)
• tamoxifen-treated MEFs treated with EBSS and the autophagic inhibitor, bafilomycin A1, show unchanged ratio of LC3B-II/LC3B-I, suggesting no effect on induction of autophagic flux but more likely autophagosome degradation
• 13-cis retinoic acid can still rescue the autophagic defects when tamoxifen-treated primary neurons are treated with AGN 194310, a RAR pan-inhibitor
• however, docosahexaenoic acid, an agonist of RXR, does not rescue the autophagic defects in tamoxifen-treated primary neurons
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• primary neurons treated with tamoxifen show an increase in the number of mitochondria in autophagosomes indicating that damaged mitochondria accumulate rather than undergo autophagic degradation
• primary neurons treated with tamoxifen and then 13-cis retinoic acid show restoration of the impaired mitophagic activity
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nervous system
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• primary neurons show an increase in the number of total mitochondria and damaged mitochondria
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• the autophagosome-lysosome fusion process in neurons is blocked in tamoxifen-treated primary neurons
• primary neurons treated with tamoxifen and then 13-cis retinoic acid show improvement of the decreased colocalization of autophagosomes and acid lysosomes, indicating partial rescue of the blocked autophagosome-lysosome fusion process in neurons
• hippocampal neurons exhibit lower oxygen consumption rates
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